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Pathological Processes > PP 1 Cell Injury And Death > Flashcards

PP 1 Cell Injury And Death Flashcards

1
Q

2 causes of cell injury

A

Environmental
Non environmental

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2
Q

Environment cause of cell injury

A

Hypoxia
Toxins/poisons
Immune mediated
Physical agents
Infection
Nutritional/dietary

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3
Q

Non environmental causes of cell injury

A

Genetics
Ageing

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4
Q

Hypoxia meaning

A

Oxygen deprivation

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5
Q

Causes of hypoxia

A

Hypoxaemic hypoxia
Anaemic hypoxia
Ischaemic hypoxia
Histotoxic hypoxia

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6
Q

What is hypoxaemic hypoxia?

A

Arterial content of O2 is low

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7
Q

What is anaemia hypoxia?
Example

A

Decreased ability of haemoglobin to carry oxygen
e.g. carbon monoxide poisoning

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8
Q

What is ischaemic hypoxia?

A

Interruption of blood supply

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9
Q

What is histotoxic hypoxia?

A

Inability to utilise O2 due to disabled oxidative phosphorylation enzyme

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10
Q

How long does it take for neurones to be affected by hypoxia?

A

A few minutes

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11
Q

why is CPR needed ASAP in cardiac arrest?

A

Neurones are affected by hypoxia after a few minutes
To prevent brain damage

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12
Q

How long does it take for skeletal muscle to be affected by hypoxia?

A

A few hours

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13
Q

Examples of toxins

A

Poison
Pollutant
Insecticides
Herbicides
Asbestos
Alcohol
Drugs

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14
Q

What is a hypersensitivity reaction?
Example

A

Injury secondary to excessive immune reaction to a non self antigen
E.g. anaphylaxis

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15
Q

Physical agents examples

A

Trauma
Extreme temp. - frost bite, burns
Electric currents
Radiotherapy

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16
Q

Types of microbes

A

Bacterial
Viral
Parasitic
Fungal

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17
Q

Nutritional/dietary issues which can cause cell injury

A

Obesity
Anorexia
Dietary deficiency or excesses - B12/folate/vit D/fat

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18
Q

Issues due to genetics/ageing

A

Inborn errors of metabolism
Enzyme deficiencies
Dysfunctional proteins

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19
Q

What happens in reversible cell damage?

A
  • swelling: due to Na+/K pump failure
  • cytoplasmic blebs
  • clumped chromatin: due to reduced pH
  • ribosome dispersion: lack of ATP to hold together
  • membrane remains intact
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20
Q

What happens in irreversible cell damage?

A
  • nuclear changes
  • membrane defects > causes lysis of ER
  • lysosome rupture
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21
Q

What is cell death due to?

A

Irreversible cell injury

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22
Q

Types of cell death

A

Apoptosis
Necrosis

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23
Q

Apoptosis meaning

A

Individual programmed cell death

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24
Q

Describe apoptosis

A

Single cell death
Cell shrinks
Plasma membrane preserved
Organelles contract
DNA cleaved between nucleosides
Dead cells taken up by phagocytosis

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25
Q

Pathways of apoptosis

A

Intrinsic (mitochondrial)
Extrinsic (death receptor)

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26
Q

Intrinsic pathway of apoptosis

A

Mitochondria released cytochrome C
Activates caspases which induce apoptosis

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27
Q

What are caspases?

A

Enzymes involved in cell death

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28
Q

Extrinsic pathway of apoptosis

A

Death receptors attach to cell membrane which activates caspases > apoptosis

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29
Q

What are death receptors secreted by?

A

T killer cells

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30
Q

Describe necrosis

A

Grouped cell death
Cell swells
Plasma membrane destroyed
Organelles swell and break down
DNA is degraded randomly
Dead cells start inflammatory process

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31
Q

Characteristic nuclear changes in necrosis

A

Pyknosis
Karyorrhexis
Karyolysis

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32
Q

What is pyknosis?

A

Nuclear shrinkage

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33
Q

What is karyorrhexis?

A

Nuclear fragmentation

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34
Q

What is karyolysis?

A

Nuclear dissolution

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35
Q

Main types of necrosis

A

Coagulative
Liquefactive

36
Q

Other types of necrosis

A

Caseous
Fat necrosis
Fibrinoid necrosis

37
Q

What type of necrosis is often a sign of TB?

A

Caseous necrosis

38
Q

Describe coagulative necrosis

A

Solid organs
Retains ghost outline of cells
Protein denaturation > release of proteases

39
Q

Describe liquefactive necrosis

A

Damage of loose tissue
Complete loss of architecture
Tissue breakdown due to release of proteases

Often in soft organs within collagenous framework e.g.brain or areas of many neutrophils

40
Q

Describe fat necrosis

A

Direct trauma onto fatty areas
Many adipocytes
e.g. Acute pancreatitis

41
Q

Molecules released by dead cells

A

Potassium
Myoglobin
Enzymes

42
Q

Who have high levels of myoglobin?

A

Extreme sports athletes
Older people after a fall
Due to over worked muscles

43
Q

What is myoglobin highly toxic to?

A

Kidneys

44
Q

What does high levels of myoglobin cause?

A

Rhabdomyolysis

45
Q

Sign of rhabdomyolysis

A

Tea coloured urine

46
Q

What could tea coloured urine indicate?

A

Rhabdomyolysis

47
Q

Gangrene meaning

A

Necrosis visible to naked eye

48
Q

Infarction meaning

A

Necrosis cause by reduction in arterial blood flow

49
Q

What can ischaemia cause?

A

Infarction

50
Q

What can an infarction cause?

A

Gangrene

51
Q

Type of gangrene

A

Dry
Wet
Gas

52
Q

What is dry gangrene due to?
What type of necrosis is seen?

A

Due to necrosis being exposed to air
Coagulative necrosis

53
Q

What is wet gangrene due to?
What type of necrosis is seen?

A

Due to necrosis being exposed to infection
Liquefactive necrosis

54
Q

What is gas gangrene due to?
What does it look like?
Where is it commonly seen?

A
  • Due to wet gangrene being infected by anaerobic bacteria
  • visible palpable bubbles of gas within tissue
  • Often in traffic accidents
55
Q

Where is gas gangrene often see?

A

Traffic accidents

56
Q

Complications of infarctions depend on…

A
  • alternative blood supply?
  • speed of ischaemia
  • tissues involved
  • O2 content of blood
57
Q

What is pathological calcification?

A

Abnormal deposition of calcium within tissues

58
Q

Types of pathological calcification

A

Dystrophic/localised
Metastatic/generalised

59
Q

Where does dystrophic calcification occur?

A

Areas of dying tissues
Atherosclerotic plaques
Within neoplastic growths
Ageing or damaged heart valves
TB lymph nodes

60
Q

Where does metastatic calcification occur?

A

Body wide
Hydroxyapatite crystals deposited in normal tissues in cases of hypercalcaemia

61
Q

Mechanisms of cell injury

A
  • depletion of ATP
  • direct mitochondrial damage
  • direct membrane damage
  • disruption of calcium homeostasis
  • oxidative stress (free radicals)
  • direct damage to DNA and proteins
62
Q

How does hypoxia cause ATP deletion?

A

1- cells deprived of oxygen
2- reduction in oxidative phosphorylation
3- mitochondrial ATP production stops

63
Q

Effect of reduction in ATP

A
  • Anaerobic glycolysis > decrease in cell pH > affects enzymes
  • ATP needed for NA+/K+ pump > cell swelling + Ca2+ enters cells > irreversible cell damage
  • Ribosomes detach from ER > reduce protein synthesis
64
Q

What does a Ca2+ influx cause?

A

Irreversible cell damage

65
Q

What does excess calcium activate?

A

ATPases
Phosphilpases
Proteases
Endonucleases

66
Q

What do ATPases do?

A

Catalyses the hydrolysis of the phosphate bond in ATP to ADP

67
Q

What do endonucleases do?

A

Breakdown DNA

68
Q

What is a free radical?

A

Atom with unaired electron

69
Q

Is necrosis always only pathological, only physiological or both?

A

Pathological only

70
Q

What are free radicals generated in?

A

Chemical/radiation injury
Cellular ageing
Anti-microbial killing by phagocytosis
Ischaemia-reperfusion injury

71
Q

What is the most dangerous free radical?

A

OH° hydroxyl

72
Q

What do free radicals damage?

A

Lipid
Protein
DNA

73
Q

What antioxidants help the body control free radicals?

A
  • free radical scavengers
  • ascrobic acid
  • glutathione GSH
74
Q

Enzymes used to control free radicals

A
  • superoxidase dismutase SOD + catalase
  • glutathione peroxidase
75
Q

How does superoxide dismutase control free radicals?

A
  • SOD: 2 superoxides > 2H2O2
  • catalase: 2H2O2 > 2H2O + O2
76
Q

Heat shock protein function

A

Help repair + refold damaged proteins
Label proteins for degeneration

77
Q

Infarction meaning

A

Necrosis due to ischaemia

78
Q

Describe caseous necrosis

A

Structureless
Reduced individuality > looks like a clump
Often in TB

79
Q

What does the body have to control free radical damage?

A

Heat shock proteins
e.g. ubiquitin

80
Q

What transport proteins are used to control free radicals?

A

Iron binds by transferrin
Calcium binds by ceruloplasmin

81
Q

What are the most common free radicals?

A

Hydroxyl
Superoxides
Hydrogen peroxide

82
Q

Where is Liquefactive necrosis often seen?

A

Often in soft organs within collagenous framework e.g.brain
Areas of many neutrophils

83
Q

Where does coagulative necrosis occur?

A

Solid organs
e.g heart, liver, kidneys, spleen

84
Q

Is there haemorrhage associated with white or red infarcts?

A

Red

85
Q

Where do white infarcts occur?
What are they due to?
What shape are they often in?
Is there associated haemorrhage?

A
  • solid organs e.g.spleen, kidney, heart
  • occlusion of end artery
  • wedge shaped
  • no associated haemorrhage
86
Q

Where do red infarcts occur?
Is there associated haemorrhage?

A
  • organs with dual blood supply e.g. intestines, lungs
  • associated with haemorrhage into dead tissue

Pathological Processes (14 decks)

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